ライフサイエンスコーパス: Phe

1 Phe accumulation had multifaceted intercompartmental eff

2 Phe has been proposed to bind, in addition to the cataly

3 Phe(59) and Tyr(101) substitutions with His and Phe, res

4 Phe(79) interacts with His(85), and Phe(79) mutants show

5 Phe, Leu, and Met are favored residues, each with a clea

6 Phe-316 and Tyr-766 variants retained catalytic activity

7 ese results were taken as evidence that B(1)-Phe-cholyl-insulin had been taken up by the ileal bile s

8 We functionally identify the HG as Val(109), Phe(150), Val(177), and Val(178), which play a critical

9 Here, we identified a Tyr-16-Phe (Y16F) change in the NS4A transmembrane domain that

10 into the peptide macrocycles c[Pro(1)-Arg(2)-Phe(3)-Phe(4)-Xaa(5)-Ala(6)-Phe(7)-dPro(8)], where Xaa w

11 e peptide macrocycles c[Pro(1)-Arg(2)-Phe(3)-Phe(4)-Xaa(5)-Ala(6)-Phe(7)-dPro(8)], where Xaa was Dap(

12 port requires URAT1 residues Cys-32, Ser-35, Phe-365 and Ile-481.

13 ted by hydrophobic interactions with Trp-37, Phe-260, and Tyr-443.

14 hetases that enable genetic encoding of SF(5)Phe for site-specific incorporation into proteins in hig

15 The potential of SF(5)Phe in protein research is illustrated by (i) increasing

16 yme by mutation of a phenylalanine to a SF(5)Phe residue, (ii) site-specifically adhering beta-cyclod

17 SF(5)Phe, para-pentafluorosulfanyl phenylalanine, is an unnat

18 residues in the core of the protein to SF(5)Phe.

19 es revealed that perturbation of the Tyr(51)-Phe(64) conformation disrupts several long-range tertiar

20 dge-to-face conformation between the Tyr(51)-Phe(64) pair of interacting aromatics is vital to the fo

21 triad of three amino acids, Phe(36)-Tyr(51)-Phe(64), is a unique SUMO signature that is absent in ot

22 c[Pro(1)-Arg(2)-Phe(3)-Phe(4)-Xaa(5)-Ala(6)-Phe(7)-dPro(8)], where Xaa was Dap(5) or Asn(5), to expl

23 interactions with the aromatic ring in N (6)-Phe-cAMP or N (6)-Bn-cAMP or a steric clash with the aro

24 A reduced apparent affinity of N (6)-Phe-cAMP toward the variants R635A and R635E strengthene

25 ladenosine-3',5'-cyclic monophosphate (N (6)-Phe-cAMP), N (6)-benzyladenosine-3',5'-cyclic monophosph

26 ological data have also shown that DISC1 607 Phe/Phe genotype was associated with higher T. gondii an

27 having e.g. 4.8% Lys, 2.7% Met+Cys, and 7.7% Phe+Tyr.

28 te, we developed a peptide, [Leu(3), Leu(7), Phe(8)]-gamma-MSH-NH2 (compound 5), which is 16-fold sel

29 [Leu(3), Leu(7), Phe(8)]-gamma-MSH-NH2 is ideal for inducing short-term s

30 se in vitro screens identified MTM(ox)32E (a Phe-Trp dipeptide-based 2'-conjugate) for in vivo testin

31 s in the absence of Phe, is different from a Phe-stabilized allosterically activated PAH tetramer.

32 cylation of tRNA(Phe) with the more abundant Phe oxidation product o-Tyr is limited by kinetic discri

33 oid receptor selective antagonist arodyn (Ac[Phe(1,2,3),Arg(4),d-Ala(8)]dynorphin A(1-11)-NH(2)) by r

34 To achieve Phe hyperaccumulation in a plant system, we simultaneous

35 that PAA is synthesized from the amino acid Phe, via phenylpyruvate.

36 similar but non-phosphorylatable amino acid (Phe) restores the more dynamic cellular functions of NMI

37 nserved aromatic triad of three amino acids, Phe(36)-Tyr(51)-Phe(64), is a unique SUMO signature that

38 orrelate to ASP loop residues, an additional Phe to Ala substitution was synthesized and observed to

39 This conformational change does not affect Phe or Tyr activation or the aminoacylation activity of

40 hile beta-ketosulfonamides derived from Ala, Phe, or hPhe gave the hydrates of the imino beta-keto-al

41 omposed of six residues (Arg-Phe-Phe-Asn-Ala-Phe) that is imperative for binding and function.

42 at the mMC4R, c[Pro-His-DPhe-Arg-Trp-Asn-Ala-Phe-DPro] and c[Pro-His-DPhe-Arg-Trp-Dap-Ala-DPro], and

43 rocyclic scaffold (c[Pro-Arg-Phe-Phe-Asn-Ala-Phe-DPro]) were explored with 14-compound and 8-compound

44 erived peptide with the sequence Ser-Val-Ala-Phe-Ser (SVAFS) displayed robust blocking activity again

45 ve loop derivative c[Pro-Arg-Phe-Phe-Xxx-Ala-Phe-DPro], where Xxx was the native Asn of AGRP or a dia

46 port, we show that a single residue of Alk5 (Phe(84)), when mutated, abolishes GDF11 signaling, but h

47 Allosteric Phe binding favors accumulation of an activated PAH tetr

48 alternative models all placed the allosteric Phe-binding module 8-10 angstrom farther from the tetram

49 Nef dimer interface (Leu(112), Tyr(115), and Phe(121)) and demonstrated attenuated homodimer formatio

50 Residues Thr-123 and Phe-382 in the catalytic domain form a latch-like intera

51 le antiparallel structures (with Asp(15) and Phe(19) aligned), are highly stable and ordered.

52 s mimicking the interactions of Phe(229) and Phe(279) of IL-6R.

53 The amino acids Glu-282 and Phe-286 near the extracellular domain on the third trans

54 tions between a residue in M3 (Tyr(309)) and Phe(167), a residue adjacent to the Cys loop FPF motif,

55 parison with FeLOX suggests that Phe-332 and Phe-525 might contribute to the unique suprafacial hydro

56 Two of these residues, Ser-35 and Phe-365, are also important for urate transport kinetics

57 rected mutagenesis revealed that Leu(46) and Phe(123) were involved in NADH binding, whereas Trp(70)

58 sensitivity, and substitutions of Glu-67 and Phe-269 altered the pH and voltage modulation of transpo

59 the respective alphaCT residues Phe(701) and Phe(705) The structure provides a platform for the furth

60 Phe(79) interacts with His(85), and Phe(79) mutants showed diminished affinity for shorter c

61 served aromatic residues Trp-71, Tyr-87, and Phe-89 at the center of this pocket.

62 ng to pI, hydrophobicity, Ser abundance, and Phe bilayer asymmetry that change across the Golgi.

63 uctures of Gly-AMP, Pro-AMP, betaPro-AMP and Phe-AMP bound to RNase A as crystallization chaperone sh

64 , the peptides Gly-Pro-Ala-Val, Val-Cys, and Phe-Phe have not been previously identified to have the

65 ar orbitals are delocalized over Chl(D1) and Phe(D1) as well as one weaker oscillator strength state

66 (59) and Tyr(101) substitutions with His and Phe, respectively, reduced LsdA activity (k (cat) (app))

67 nalysis highlighted highly conserved Ile and Phe residues at the RfaH interdomain interface.

68 acid in PSLFQ to Ala identified both Leu and Phe as independently essential for MGAT4D-L activity.

69 ions between the last residue of post-M4 and Phe(170) of the conserved FPF sequence of the Cys loop,

70 conserved phenylalanine (Phe-202 (Mfn1) and Phe-223 (Mfn2)) located in the GTPase domain on a conser

71 similar in S. venezuelae OtsA (Asp, Ser, and Phe, respectively) but not conserved in E. coli OtsA (Hi

72 hanced aromatic sequons (Phe-X-Asn-X-Thr and Phe-X-X-Asn-X-Thr), which can be efficiently N-glycosyla

73 Using misacylated Pro-tRNAPhe and Phe-tRNAPro, we show that the imino acid proline and not

74 synthesized analogue, Ac-Arg-Ala-[d-Cys-Arg-Phe-His-Pen]-COOH (19), displayed subnanomolar affinity

75 plasma stable peptide, Ac-Arg-Ala-[d-Cys-Arg-Phe-Phe-Cys]-COOH (3).

76 For both ASP and AGRP, the hypothesized Arg-Phe-Phe pharmacophores are on exposed beta-hairpin loops

77 hexapeptide H(2)N-(CH(2))(4)-CO-Pro-Leu-Arg-Phe-Gly-Ala-NH-CH(2)-Fc is the optimal probe for catheps

78 eported AGRP macrocyclic scaffold (c[Pro-Arg-Phe-Phe-Asn-Ala-Phe-DPro]) were explored with 14-compoun

79 in the AGRP active loop derivative c[Pro-Arg-Phe-Phe-Xxx-Ala-Phe-DPro], where Xxx was the native Asn

80 a-hairpin loop composed of six residues (Arg-Phe-Phe-Asn-Ala-Phe) that is imperative for binding and

81 or tripeptide DPhe-Arg-Trp replaced the Arg-Phe-Phe sequence in the AGRP active loop derivative c[Pr

82 ution of various planar (including aromatic (Phe, Trp, Tyr, and His)/amide (Asn and Gln)/Guanidine (A

83 etaF as well as several side chains, such as Phe-57, Tyr-60, and Ile-77, that change their orientatio

84 f intrinsically disordered proteins, such as Phe-Gly repeat domains, alters drastically when they are

85 A key patch of amino acids, Asp-Phe-Asp (the 'DFD patch'), situated at the mouth of the

86 with type I inhibitors assume an active "Asp-Phe-Gly (DFG)-in" and "alphaC-in" conformation.

87 ent of TCam-2 cells with the peptide Leu-Asp-Phe-Ile (LDFI), a full leptin-receptor antagonist, compl

88 1 ((177)Lu-DOTA-dGlu-Ala-Tyr-Gly-Trp-Met-Asp-Phe-NH(2)) and (177)Lu-DOTA-PP-F11 ((177)Lu-DOTA-(dGlu)(

89 77)Lu-DOTA-(dGlu)(6)-Ala-Tyr-Gly-Trp-Met-Asp-Phe-NH(2)), and whether the use of protease inhibitors f

90 77)Lu-DOTA-(dGlu)(6)-Ala-Tyr-Gly-Trp-Nle-Asp-Phe-NH(2)) performs better than reference analogs with v

91 ontributions of the activation loop, the Asp-Phe-Gly (DFG) motif, the regulatory spine, and the gatek

92 Examination of aza-Gly-Pro and aza-Phe-Pro analogs 2a and 2b in a murine preterm labor mode

93 in the substrate C3 pocket with the bulkier Phe enhances stereoselectivity (cis:trans ~99:1), wherea

94 ics simulation data suggested that the bulky Phe acts as a pawl that stabilizes the downward ratchet-

95 P remains intact but cannot be attenuated by Phe.

96 s obtained with MeJ application, followed by Phe+MeJ; while Phe treatment barely increased phenolic c

97 usly identified for allosteric inhibition by Phe.

98 When Trp is replaced by Phe, protons can be transferred to H37 bidirectionally w

99 terocyclic inhibitors (PVHIs) containing Cbz-Phe-Phe/homoPhe scaffolds with vinyl-2-pyrimidine, vinyl

100 ive molecules and the amino acid side chains Phe, Tyr, and Trp.

101 , N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N,N-di-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala were identi

102 while Phe-Gly formed only N-Cl-/ N, N-di-Cl-Phe-Gly.

103 table in water over 10 days except N,N-di-Cl-Phe-Gly.

104 N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N,N-di-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-

105 N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala along with

106 I)DPhe" motif with respect to the classical "Phe-Arg" melanocortin signaling motif, which results in

107 d during oxidative stress, while the cognate Phe-tRNA(Phe) aminoacylation activity is unchanged.

108 the alphaI alpha1-helix contains a conserved Phe.

109 s quite unusual in that the highly conserved Phe in the DFGpsi motif, which is 1 of the 4 R-spine res

110 different enzymatic functions and converted Phe into 2-phenylethylamine and 2-phenylacetaldehyde, re

111 obe of TPETH-2(CFTERD3) (where CFTERD is Cys-Phe-Thr-Glu-Arg-Asp) was developed for chymase detection

112 tifs such as d-Pro-Gly, both the 2-Abz and d-Phe rings may be further functionalized.

113 he structural formula of the native L3P as D-Phe-N-Methyl-L-Val-L-Ala-OMe attached in N-ter to a 20-c

114 nity of the decapeptide Gramicidin S cyclo(d-Phe-Pro-Val-Orn-Leu-)2 (GS).

115 lding blocks to the GRPR-selective ligand [d-Phe(6), beta-Ala(11), Ala(13), Nle(14)]Bn(6-14) (sBB2L)

116 calorimetry (ITC), we studied a series of d-Phe/d-DiPhe-Pro-(amino)pyridines.

117 ith the GRPr antagonists HZ219, DOTA-PEG4-[D-Phe(6), Sta(13)]-BN(6-14)NH2 (DOTA-AR), and DOTA-(4-amin

118 ]-BN(6-14)NH2), by reacting DOTA-Lys-PEG4-[D-Phe(6), Sta(13)]-BN(6-14)NH2 (HZ219) with IRDye 650 N-hy

119 tagonist, HZ220 (DOTA-Lys(IRDye 650)-PEG4-[D-Phe(6), Sta(13)]-BN(6-14)NH2), by reacting DOTA-Lys-PEG4

120 DOTA-(4-amino-1-carboxymethyl-piperidine)-[D-Phe(6), Sta(13)]-BN(6-14)NH2 (DOTA-RM2).

121 ed DOTA-4-amino-1-carboxymethyl-piperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is

122 The d-Phe-2-Abz turn may serve as a tool for the synthesis of

123 idine A, (Tyrc A) was substituted with the d-Phe-2-aminobenzoic acid (2-Abz) motif in a synthetic ana

124 The d-Phe-Pro beta-turn of the cyclic beta-hairpin antimicrobi

125 The inhibitors carbobenzoxy (Z)-d-Phe-l-Phe-Gly (fusion inhibitor peptide [FIP]) and 4-nit

126 Other homologues, such as Z-d-Phe, are less effective but may act through the same mec

127 cades ago, the small hydrophobic peptide Z-d-Phe-l-Phe-Gly (FIP) was shown to block MeV infections an

128 e resistant to the inhibitory effects of Z-d-Phe-l-Phe-Gly.

129 d exciton-charge transfer states (Chl(D1) (+)Phe(D1) (-))* and (P(D2) (+)P(D1) (-))*.

130 the residue before the DFGmotif, and the DFG-Phe side-chain rotamer, utilizing a density-based cluste

131 titution of three amino acids in CsGA1ox/ds, Phe(93), Pro(106), and Ser(202), with those typically co

132 Phe derivatives; however, how plants endure Phe accumulating conditions in the absence of an excreti

133 aration of the BM2 channel using fluorinated Phe-5.

134 Results showed that foliar Phe and MeJ treatments decreased the concentration of mo

135 t pH 6.5 and temperature of 40 degrees C for Phe-pNA as a substrate.

136 er to increase expression of the enzymes for Phe production or to have altered transporters, which li

137 ble the integration of allosteric input from Phe and provide a paradigm for the coordinate regulation

138 ion of several amino acids than samples from Phe and MeJ applications.

139 to inhibit human LTalpha is caused by a Glu-Phe-Glu motif in its 90s loop.

140 quantification of three dipeptides, Tyr-Gly, Phe-Gly, and Tyr-Ala, from raw water demonstrates a usef

141 cognizes the pan-opioid sequence Tyr-Gly-Gly-Phe at the N terminus of most endogenous opioid peptides

142 Here we show that the gp120 Phe 43 cavity modulates the propensity of Env to sample

143 tophan for serine 375 (S375H/W) in the gp120 Phe 43 cavity, where Phe 43 of CD4 contacts gp120, resul

144 ot depend upon the availability of the gp120 Phe 43 cavity.

145 condensation reaction of the resulting HOOC-Phe-SWCNT with 1-(3-aminoethyl)-4,4'-bipyridinium bromin

146 f an LsdA.phenylazophenol complex identified Phe(59), Tyr(101), and Lys(134) as contacting the 4-hydr

147 ); copper complexes with phenylanine: Cu(II)(Phe)(2) and Cu(II)(Phe)(3) and nicotianamine: Cu(II)(NA)

148 with phenylanine: Cu(II)(Phe)(2) and Cu(II)(Phe)(3) and nicotianamine: Cu(II)(NA); zinc complexes wi

149 The most frequent mutation, resulting in Phe-508 deletion, causes CFTR misfolding and its prematu

150 led to an 18-fold expansion of the internal Phe pool.

151 L-Phe-mediated allosteric activation induces a repositioni

152 lific producer of the essential amino acid L-Phe, which we identified as an agonist for GPR56 and GPR

153 acids resulted in the identification of an l-Phe ester that offered an improved exposure of 1 and red

154 aracteristics of polydopamine imprinted by L-Phe biomarker drastically increase the light trapping an

155 56 and GPR97; and a species that converted L-Phe into the potent psychoactive trace amine phenethylam

156 ld-type hPAH is lacking, we addressed hPAH L-Phe-mediated conformational changes and report the first

157 Marfey and Mosher indicated l-Glu, l-Ile, l-Phe and 1S-configurations, respectively; ROESY correlati

158 ed in the discovery of the self-immolative l-Phe-Sar dipeptide derivative 74 that gave four-fold impr

159 ymerization of dopamine in the presence of L-Phe as biomarker.

160 ed superb performance for the detection of L-Phe biomarker in the optimized condition obtained from c

161 Binding of L-Phe induces a large movement and dimerisation of regulat

162 the active site entrance in the absence of L-Phe.

163 ago, the small hydrophobic peptide Z-d-Phe-l-Phe-Gly (FIP) was shown to block MeV infections and sync

164 The inhibitors carbobenzoxy (Z)-d-Phe-l-Phe-Gly (fusion inhibitor peptide [FIP]) and 4-nitro-2-p

165 stant to the inhibitory effects of Z-d-Phe-l-Phe-Gly.

166 curate quantifications of L-phenylalanine (L-Phe) in plasma and whole-blood newborns samples diagnose

167 ylase (hPAH) hydroxylates L-phenylalanine (L-Phe) to L-tyrosine, a precursor for neurotransmitter bio

168 To maintain physiological L-Phe levels, hPAH employs complex regulatory mechanisms.

169 This work suggests that such L-Phe-imprinted polydopamine-coated Zn/CdS/CdSe heterojunc

170 cular dynamics simulations indicating that L-Phe binding and mutation of the conserved N-terminal Trp

171 chemotactic migration toward formyl-Met-Leu-Phe (fMLP) and stromal cell-derived factor 1alpha (SDF-1

172 taxis towards chemoattractant formyl Met-Leu-Phe (fMLP) coupled with their decreased polarization, an

173 oli and the chemoattractant N-formyl-Met-Leu-Phe (fMLP)-coated beads.

174 ed neutrophil chemotaxis to a formyl-Met-Leu-Phe gradient.

175 the AnxA1 pathway (by using N-t-Boc-Met-Leu-Phe, a nonselective AnxA1 receptor antagonist, or by usi

176 ed recombinant protein, we show that the Leu-Phe substitution increases turnover rate of acetaldehyde

177 s of His583 to Ala, Asp, Asn, Glu, Gln, Lys, Phe, Tyr, and Trp showed that although both the Cu(Z) an

178 losteric regulation is necessary to maintain Phe below neurotoxic levels.

179 MeJ+Phe treatment did not affect must nitrogen content.

180 nylalanine (Phe) as a precursor feeding (MeJ+Phe) and its application individually on must amino acid

181 Musts obtained from MeJ+Phe showed higher concentration of several amino acids t

182 we discovered a four-residue pi-clamp motif (Phe-Cys-Pro-Phe) for regio- and chemoselective arylation

183 In this study, we found that mutating Phe(20) to cyclohexylalanine (Cha) in macrocyclic Abeta-

184 domain through incorporation of noncanonical Phe analogs with distinct electrostatics at two position

185 tetramer, which dominates in the absence of Phe, is different from a Phe-stabilized allosterically a

186 tructure both in the presence and absence of Phe, which serves as both substrate and allosteric activ

187 Accumulation of Phe did not lead to an increase in flux toward phenylace

188 imarily intact protein and a small amount of Phe.

189 during infection, including the cleavage of Phe/Gly-containing nucleoporin proteins (Nups) within nu

190 fusion in vitro, we found that conversion of Phe-202 to leucine in either Mfn1 or Mfn2 diminishes the

191 at catalyze the non-oxidative deamination of Phe to trans-cinnamic acid, the committed step for the m

192 Deletion of Phe(508) (DeltaF508), the most prevalent mutation in CF,

193 n on graphene due to an even distribution of Phe residues and hydrophilic residues.

194 oach between PS2 and the phenyl ring edge of Phe-232 that is surrounded by pairs of lysines and argin

195 ) that contributes to sequestering excess of Phe in the vacuole.

196 enylketonuria, are mitigated by excretion of Phe derivatives; however, how plants endure Phe accumula

197 by NOE spectroscopy, shows the importance of Phe and Arg interactions in driving the phase separation

198 The diet restricts intake of Phe from natural proteins in combination with traditiona

199 of IL-6, thus mimicking the interactions of Phe(229) and Phe(279) of IL-6R.

200 ld increase in the rate of mistranslation of Phe codons as Tyr compared to wild type, the increase in

201 the committed step for the major pathway of Phe metabolism.

202 of a distinct metabolically inactive pool of Phe, likely localized in the vacuole.

203 o 42 (12.2%) when assayed in the presence of Phe-Arg-beta-Napthylamide, with 35 of these 42 possessin

204 Reversion of Phe(87) to tyrosine abolished GABA's inhibitory effect a

205 Since only subsets of Phe/Gly motifs, particularly those within Nup62, Nup98,

206 ring effects were blunted by substitution of Phe for Tyr-67 in FXR.

207 Substitution of Phe-269, located close to the substrate-binding site, al

208 ating the hypothesis that the ADT3 supply of Phe is required to control ROS concentration and distrib

209 (Populus trichocarpa) produces a variety of Phe-derived metabolites, including 2-phenylethylamine, 2

210 Thus, replacement of either Leu-395 or Phe-396 with Ala led to inactivation of MGAT4D-L inhibit

211 Introducing Trp(85) or Phe(29) to replace Cys or Leu, respectively, disrupts pa

212 free KLK2 toward peptidic substrates with P2-Phe, the situation was reverted toward protein substrate

213 on of the aromatic amino acid phenylalanine (Phe) in animals, known as phenylketonuria, are mitigated

214 jasmonate (MeJ) supported by phenylalanine (Phe) as a precursor feeding (MeJ+Phe) and its applicatio

215 nd Mfn2 paralogs, a conserved phenylalanine (Phe-202 (Mfn1) and Phe-223 (Mfn2)) located in the GTPase

216 t addition of the inhibitor L-phenylalanine (Phe) prevents maximal activation of FBP-bound PKM2 tetra

217 Vine foliar applications of phenylalanine (Phe) or methyl jasmonate (MeJ) could improve the synthes

218 c activation by the substrate phenylalanine (Phe); the allosteric regulation is necessary to maintain

219 ce of a critical role for the phenylalanine (Phe) biosynthetic activity of AROGENATE DEHYDRATASE3 (AD

220 ted by precursor feeding with phenylalanine (Phe), in order to improve Garnacha grape phenolic conten

221 lalanine (Tyr-Ala), and phenylalanylglycine (Phe-Gly), reacted with sodium hypochlorite, and these re

222 ee aromatic dipeptides, phenylalanylglycine (Phe-Gly), tyrosylalanine (Tyr-Ala), and tyrosylglycine (

223 AA-MFs decreased plasma Phe (-85 +/- 40 mumol/L, P = 0.044) with stable Phe inta

224 A nanobody containing an Asn-Pro-Phe peptide within the complementarity-determining regio

225 d a four-residue pi-clamp motif (Phe-Cys-Pro-Phe) for regio- and chemoselective arylation of cysteine

226 opic offsets among AAs (e.g. Delta(15) N(Pro-Phe) ), to explore the allocation of endogenous versus e

227 The value of emperor penguin Delta(15) N(Pro-Phe) was higher in yolk and albumen than in muscle, refl

228 in comparison, the value of Delta(15) N(Pro-Phe) was similar across muscle and egg tissue in previou

229 This Pro-Phe Met relay may constitute a structural switch that me

230 FtsZ CTD residue Phe-377 inserts into the ZapD pocket, anchoring the CTD

231 identical to the respective alphaCT residues Phe(701) and Phe(705) The structure provides a platform

232 Tyr(274) interacting with IFN-beta residues Phe(63), Leu(64), Glu(77), Thr(78), Val(81), and Arg(82)

233 pocket, comprising the hydrophobic residues Phe-1012, Val-1025, Tyr-1089, and Leu-1092).

234 have focused on OleTJE active site residues Phe(79), His(85), and Arg(245) to interrogate their role

235 Mutating SM residues Phe-35/Ser-37/Leu-65/Ile-69 into alanine, based on the k

236 ts in which two conserved aromatic residues (Phe(3049) and Trp(3052)) were either individually or bot

237 t the hypothesis that two aromatic residues (Phe-174 and Trp-376), conserved in bacterial GEs, intera

238 ructures revealed that two pol eta residues, Phe-18 and Tyr-92, behave as steric gates to influence s

239 f the few nonconserved active-site residues, Phe(201) in P. aeruginosa IGPS, is by mutagenesis demons

240 with mutations in four active-site residues, Phe-316, His-583, Tyr-766, and His-767.

241 T) sequon and the enhanced aromatic sequons (Phe-X-Asn-X-Thr and Phe-X-X-Asn-X-Thr), which can be eff

242 of the fluorogenic substrate hydrodabcyl-Ser-Phe-EDANS by the proteases thermolysin and papain.

243 (-85 +/- 40 mumol/L, P = 0.044) with stable Phe intake.

244 ing the P1 Tyr residue with para-substituted Phe derivatives, generating new inhibitors with improved

245 ield generated by basic residues surrounding Phe-232 is key to the polarization of the PS2 moiety.

246 faster than Ala-AMP and 120-fold faster than Phe-AMP.

247 predicted NAD(+)-binding site revealed that Phe(727), Arg(757), and Arg(780) are essential for NAD(+

248 Results showed that Phe+MeJ treatment did not improve phenolic content to a

249 Comparison with FeLOX suggests that Phe-332 and Phe-525 might contribute to the unique supra

250 The Phe, Ala, and Dap/Asn residues were successively removed

251 ; B, beta; L, left) of the XDF motif and the Phe rotamer (minus, plus, trans).

252 del, we found that the residue volume at the Phe position in the alpha1-helix is critical for alphaLb

253 Here we investigate the influence of the Phe 43 cavity on ADCC responses.

254 ding mode in which the alpha-hydrogen of the Phe residue is positioned over the heme prosthetic group

255 e conformations based on the location of the Phe side chain (DFGin, DFGout, and DFGinter or intermedi

256 s focusing on two pathogenic variants of the Phe-53 residue, which maps to the well-characterized neg

257 g bis-THF of darunavir on either side of the Phe-Phe isostere of lopinavir in combination with hydrop

258 se complex regardless of the position on the Phe-Phe isostere.

259 alphaLbeta2 activation because trimming the Phe by small amino acid substitutions abolished alphaLbe

260 active and inactive conformations where the Phe residue is in contact with the C-helix of the N-term

261 n to hydroxylate two remote sites within the Phe residue of its diketopiperazine substrate thaxtomin

262 A functional role of this Phe is structurally unpredictable.

263 d in petunia flowers expression of all three Phe ammonia lyase (PAL) isoforms that catalyze the non-o

264 f interaction partners for Tyr(187) in TMIV (Phe(171)) and TMV (Trp(194)).

265 orresponding to the sequence from Asp(15) to Phe(19) of human calcitonin and reported as the minimal

266 extends seven helical turns, from Pro-405 to Phe-431, and is flanked by unstructured loops.

267 d aromaticity of the side group analogous to Phe-2 of ritonavir and demonstrated the leading role of

268 mutation of the XPA residue corresponding to Phe-262 in Rad14, previously reported as being critical

269 , for example, mutating all Tyr1 residues to Phe (Y1F) is lethal in vertebrates but a related mutant

270 re otherwise equivalent in their response to Phe, further supported by their behavior on various chro

271 Importantly, Tyr to Phe substitution renders the kinase inactive, jeopardizi

272 of the edge-to-face conformation by a Tyr to Phe substitution significantly decreased stability, SUMO

273 The Tyr-to-Phe substitution in Y(898)KAI reduced BRI1 internalizati

274 vitro assays confirmed PhCAT2 can transport Phe, and decreased PhCAT2 expression in PAL-RNAi transge

275 d these modules would produce the tripeptide Phe-N-Methyl-Val-Ala with a lipid moiety, termed lipotri

276 hermus thermophilus 70S ribosome with a tRNA(Phe) bound to a PsiUU codon in the A site supports these

277 iting, cellular levels of aminoacylated tRNA(Phe) were elevated during amino acid stress, whereas in

278 diting lowered the amount of deacylated tRNA(Phe) in the cell.

279 mt-tRNA(Val) , and mildly increased mt-tRNA(Phe) , in subjects compared with unrelated age- and sex-

280 binds 16S mt-rRNA, mt-tRNA(Met), and mt-tRNA(Phe), and we demonstrate that it is responsible for pseu

281 s cerevisiae that PheRS misacylation of tRNA(Phe) with the more abundant Phe oxidation product o-Tyr

282 oxidative stress, while the cognate Phe-tRNA(Phe) aminoacylation activity is unchanged.

283 erivative m-Tyr after its attachment to tRNA(Phe) We now show in Saccharomyces cerevisiae that PheRS

284 proofreading activity to hydrolyze Tyr-tRNA(Phe) is increased during oxidative stress, while the cog

285 In near-cellular conditions, yeast tRNA(Phe) and E. coli tRNA(Ala) transcripts fold in a single,

286 re composed of Val, Pro, Tyr, Met, Leu, Trp, Phe, Lys and Glu.

287 with SVBP, exhibited robust and specific Tyr/Phe carboxypeptidase activity on microtubules.

288 CRF01_AE HIV-1 strains have an unusual Phe 43 cavity-filling His 375 residue, which increases t

289 The methodology involved preparation of V-Phe-SWCNT(-HRP)-anti-TGF conjugates by covalent linkage

290 covalent linkage of HRP and anti-TGF onto V-Phe-SWCNT hybrids.

291 The V-Phe-SWCNT hybrids were characterized by using different

292 TGF-beta1 with signal amplification using V-Phe-SWCNT(-HRP)-anti-TGF conjugates as carrier tags.

293 (S375H/W) in the gp120 Phe 43 cavity, where Phe 43 of CD4 contacts gp120, results in the spontaneous

294 minal lobe-and DFGout-an inactive form where Phe occupies the ATP site exposing the C-helix pocket.

295 model of PAH allosteric regulation, whereby Phe binds to PAH-RD and mediates the dimerization of reg

296 in flux toward phenylacetaldehyde, for which Phe is a direct precursor.

297 a mechanism for allosteric coupling in which Phe(151) is the central residue in a hydrophobic interac

298 i-I-, and N-Cl-3-I-tyrosyl dipeptides, while Phe-Gly formed only N-Cl-/ N, N-di-Cl-Phe-Gly.

299 MeJ application, followed by Phe+MeJ; while Phe treatment barely increased phenolic compounds.

300 could be supported by precursor feeding with Phe, when both applied together.

301 ACE prefers to cleave substrates with Phe or Leu at the C-terminal P2' position and Gly in the